Cirrhosis is a chronic and irreversible chronic liver disease, characterized by the presence of fibrosis and the formation of regeneration nodules, which lead to an alteration of the vascular architecture, as well as liver function. It represents the final stage of numerous diseases that affect the liver. Regardless of the etiology of liver damage, cellular mechanisms that lead to cirrhosis are common.
The stellate or perisinusoidal cell has been implicated in the initiation and maintenance of the fibrotic changes that ultimately lead to cirrhosis.
As consequences of these histological changes suffered by the liver, there are two symptoms or clinical manifestations of cirrhosis: hepatocellular insufficiency and portal hypertension.
Can Decompensated Cirrhosis Be Reversed?
The possibility of performing a specific therapy on the etiology of cirrhosis is limited, since it is relatively frequent that the disease is diagnosed when it is already advanced.
In the case of alcoholic cirrhosis, it is important that the patient abandons the alcohol, although unfortunately this does not mean the remission of the disease; a similar situation is also presented for cirrhosis of viral origin. The effect of specific therapies such as antivirals (hepatitis B and C in early stages prior to the development of cirrhosis), D-penicillamine to chelate copper (Wilson’s disease), immunosuppressants (cirrhosis of autoimmune origin) and ursodeoxycholic acid (cirrhosis due to cholestasis), is quite limited, and is even contraindicated in viral cirrhosis once the diagnostic confirmation by biopsy is obtained. Rest and a diet for patients with liver disease are advised:
- Intake of animal protein: 0.5 g/kg of weight.
- Restriction of sodium depending on the electrolytes present in urine.
- Restriction of liquid intake to 1200 ml/day.
It is important to avoid the states of malnutrition, being able to value the introduction of vitamin complexes in case there are deficiency states, mainly vitamins B, C, K and folic acid. Hepatoprotectors are not necessary.
In any case, the definitive therapy of cirrhosis is liver transplantation.
Currently the survival of transplanted patients after 5 years stands at 80%. However, we must not forget that the surgical risk in the cirrhotic patient, and especially the abdominal surgery necessary for the transplantation, it is elevated, which means that surgery must be reserved for situations in which its non-realization carries a mortal risk for the patient. It is fundamental, therefore, to optimize the treatment of patients with cirrhosis, both to improve their quality of life and to prevent more serious complications and minimize the risks of liver transplantation.
The Following Is A Brief Analysis Of The Therapeutic Approach Of The Major Complications Of Liver Cirrhosis:
There are clearly distinguished two phases of the disease, whose chronology and prognostic markers are different: compensated cirrhosis and decompensated cirrhosis.
In relation to the prognosis, compensated cirrhosis can evolve decompensated, while the worsening of the latter leads to increased risk of death. With regard to compensated cirrhosis, the most striking is its oligosymptomatic character, with the presence of nonspecific symptoms. At 10 years, the survival of patients who remain in this phase is close to 80%. The presence of portal hypertension in this phase is considered a prognostic factor of mortality.
The appearance of ascites, variceal hemorrhage, hepatic encephalopathy and jaundice marks the beginning of the decompensated phase. When the disease evolves until reaching this stage, the survival of patients after the 10 years is at 7%. The prognosis of some of the complications of cirrhosis, as is the case with esophageal varices, has improved notably in recent years: drugs that reduce portal pressure and advances in endoscopic techniques (multi-band linker) are some of the therapeutic options that have allowed this advance.
Given the limitations of existing treatments, new potential therapeutic targets are being sought to reverse the cirrhosis.